Non-alcoholic fatty liver disease: stages of the disease, clinical manifestations, diagnosis and treatment. Alcoholic and non-alcoholic fatty liver disease – we also take into account cavity digestion Non-alcoholic fatty liver disease at the stage of steatosis

Non-alcoholic fatty liver disease (NAFLD), or steatosis, fatty hepatosis, steatohepatosis is a disease in which neutral fat accumulates in liver cells, destroying them. Risk factors are excess weight and insulin resistance due to type 2 diabetes. However, NAFLD often affects thin people as well. This disease can lead to complications if you do not see a doctor in time and start effective treatment.

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  Reasons

  Non-alcoholic fatty liver disease (NAFLD) is a pathology in which the cells of the organ are filled with neutral fats that impair function. Subsequently, hepatocytes burst due to excess lipids, and in their place first fibrosis and then cirrhosis are formed. Functionally active tissue decreases, and other metabolic disorders appear. In the classification of liver diseases, this pathology is given a separate place.

  The main reasons for the development of lipid infiltration:

  • Metabolic disorders in insulin resistance - metabolic syndrome with obesity.
  • Chronic diseases of the gastrointestinal tract.
  • Intoxication with heavy metals, pesticides, and other poisons.
  • Taking medications - oral contraceptives, glucocorticoids, antibiotics, nicotinic acid, statins.
  • Poor nutrition, sudden weight loss or weight gain.
  • Viral hepatitis.

  

  Fatty liver hepatosis - causes, symptoms, treatment, folk recipes and diet

  Treatment

  Fatty hepatosis is a serious disease that can lead to cirrhosis if treatment is not prescribed on time. There is good news - the disease is successfully corrected with the help of a balanced diet, as well as taking hepatoprotectors and folk remedies.

  An important role in the treatment of lipid degeneration is played by the normalization of metabolism and digestive processes.

  

  Hepatoprotectors

  There are many hepatoprotectors with different mechanisms of action.

  For steatotic liver degeneration, lipotropic compounds are used that utilize neutral fat from hepatocytes. Their chemical composition is characterized by the presence of methyl groups.

  

  The main drugs for the treatment of lesions in the stage of steatosis:

  • Heptral.
  • Essential lipids (Rezalut, Essentiale forte, Essliver, Phosphogliv).
  • Milk thistle extract (Silimar, Karsil, Gepabene).
  • Vitamins – folic acid, methylcobalamin, vitamin U.
  • Preparations of urso- and chenodeoxycholic acid (Henofalk, Ursofalk, Ursoliv, Livodexa, Urdoxa).

  

  Fatty liver infiltration - main signs, diagnosis and treatment

  Heptral

  This is a lipotropic compound called S-adenosylmethionine. Present and synthesized in the body, it is necessary for the production of new cells as a donor of labile methyl groups. Participates in the synthesis of various neurotransmitters and other important substances. Therefore, in case of steatohepatosis, it relieves symptoms such as lethargy, depression, apathy, and joint problems.

  S-adenosylmethionine promotes the utilization of neutral fat from liver cells and normalizes lipid metabolism. Reverses the process of fatty infiltration, preventing fibrosis and cirrhotic changes. Has a positive effect on detoxification function. Improves the storage of glucose in the form of glycogen - in diabetes mellitus, it reduces its level in the blood by maintaining liver cells.

  Available in the form of tablets and injection solutions. In intravenous and intramuscular injections, the bioavailability of the drug Heptral is 95%, while only 5% is absorbed in the digestive tract.

  Essential phospholipids

  The chemical name is phospholipids, which include several classes of compounds - phosphotidylcholine (lecithin), phosphotidylinositol, phosphotidylserine.

  These drugs are lipotropic compounds that promote the disposal of lipids accumulated in cells and causing fatty liver degeneration. Having methyl groups in their composition, they promote the processes of organ regeneration and detoxification.

  Essential lipids improve the absorption of fats, being emulsifiers, normalize digestive processes, having a choleretic effect. With fatty degeneration of the liver tissue, the gastrointestinal tract suffers, and the tendency to form gallstones increases. Lecithin helps reduce cholesterol levels in bile, making it less viscous.

  Phosphotidylinositol increases the sensitivity of cellular receptors to the action of insulin, which is important in metabolic syndrome - type 2 diabetes.

  Phosphogliv contains glycyrrhizic acid, which prevents the proliferation of viruses in steatohepatitis.

  Milk thistle

  A plant whose extract has a hepatoprotective effect. Has a choleretic effect. It is an antioxidant - this is necessary when glutathione is depleted in the liver, which occurs due to intoxication.

  

  Improves digestion and absorption of fat-soluble vitamins, as it stimulates the flow of bile. Normalizes protein synthesis in the liver, preventing edema. Promotes the formation of glycogen from excess blood glucose, which is important for metabolic syndrome.

  Used as an additional remedy for fatty degeneration. It has a positive effect on metabolism in polycystic ovary syndrome, which often accompanies steatosis in women.

  Silimar, Karsil, Legalon contain milk thistle extract, and Gepabene also contains fume extract.

  Vitamins

  Among them there are also lipotropic compounds. Fatty hepatosis in digestive diseases is caused by a deficiency of such important cofactors as methylcobalamin (B12) and folic acid. Without them, the restoration of liver cells is slow, and neutral fat is deposited intensively in hepatocytes.

  Atrophic gastritis, increased bacterial contamination of the small intestine causes a deficiency of cobalamin - external Castle factor. In this case, anemia and enlargement of the liver and spleen develop.

  Antibiotics and sulfonamides interfere with the metabolism of folic acid. Triglycerides, that is, neutral fats, can accumulate in the liver after such therapy.

  The vitamin-like compound choline improves lipid metabolism, increases cell sensitivity to insulin, which promotes glucose utilization. Contained in agrimony - a medicinal plant.

  Vitamin U – thioctic or lipoic acid. Used for detoxification in case of poisoning with heavy metals and other poisons. It has a lipotropic effect in steatohepatosis. Prescribed for type 2 diabetes mellitus as an antihypoxic agent and to reduce insulin resistance.

  Bile acids

  Ursoliv, Ursosan, Ursofalk, Henofalk - bile acids. They have a complex effect on fatty infiltration:

  • Protect cells from damage.
  • They have a choleretic effect, suppress the proliferation of microflora in the small intestine - SIBO, which plays an important role in the pathogenesis of steatosis.
  • Reduce cholesterol levels by optimizing fat metabolism.

is a descriptive term used to identify the accumulation of fat droplets in the liver cells and includes a set of specific symptoms that characterize the accumulation of fat and inflammation of the liver tissue.

Most often, this process is diffuse in nature, i.e. covers the entire liver, but there may also be a local detection of the process (lipoma) - during ultrasound examination of the abdominal organs (ultrasound). Subject to availability non-alcoholic steatohepatitis a diagnosis can be made - fatty liver degeneration, chronic hepatitis of unspecified etiology, unspecified cirrhosis of the liver. The prevalence ranges from 10 to 40%.

Risk groups for liver steatosis

• Patients with metabolic syndrome (type 2 diabetes mellitus, obesity, increased cholesterol and triglycerides).
• Patients with type 2 diabetes mellitus (in 70-100% of cases).
• Obese patients (in 30-100% of cases).
• Patients with elevated cholesterol and triglyceride levels (20-90%).
• Patients with diabetes mellitus and obesity (steatohepatitis is detected in 50% of cases, liver cirrhosis in 19-20% of cases).

Most often, patients aged 40-60 years are susceptible to the disease, but in children with normal body weight non-alcoholic fat disease detected in 2.6%, in obese children - in 22.5-52.8%.

Depending on gender, the disease predominates in women - 53-85%. First stage – fatty liver disease– 5 times more common in men, and steatohepatitis– 3 times more often in women.

Causes of non-alcoholic steatohepatitis

• Taking certain medications (hormones (glucocorticosteroids), estrogens, nefidipine, methotrexate, aspirin, diltiazem).
• Eating disorders (fasting, rapid weight loss, low protein diet).
• Surgical interventions (stomach and intestinal operations).
• External exposure to toxic substances (organic solvents, phosphorus, poisonous mushrooms).
• Intestinal diseases (inflammatory diseases, malabsorption, excessive growth of bacteria in the intestines).
• Insulin resistance is a decrease in the biological response to one or more effects of insulin.

The development of insulin resistance is facilitated by a hereditary factor - a predisposition to diabetes mellitus, detection of diabetes mellitus in close relatives, as well as excess caloric nutrition and low physical activity. These factors themselves contribute to increased obesity and fat accumulation in liver tissue. In approximately 42% of patients, risk factors for developing the disease cannot be identified.

Symptoms of non-alcoholic fatty liver disease

Most patients have no complaints. There may be discomfort and heaviness in the abdomen, weakness, increased fatigue, heaviness in the right hypochondrium, nausea, belching, and loss of appetite.

Upon examination, an increase in the size of the liver is revealed. Often there is suspicion of non-alcoholic fatty liver disease Diagnosed by performing an ultrasound of the abdominal organs or a biochemical blood test.

Diagnosis of non-alcoholic fatty liver disease

IN biochemical blood test There is an increase in liver enzymes ALT and AST to 4 norms, alkaline phosphatase to 2 norms.

At ultrasound examination (ultrasound) The information content of the method decreases in obese patients.

Computed tomography (CT) – allows you to accurately assess the degree steatosis, the sensitivity and specificity of the method is 93-100%.

Magnetic resonance imaging (MRI) – provides a complete image of the organ in any projection, has a high agreement with the data of histological examination.

Liver elastography – has higher accuracy in advanced stages of liver damage (fibrosis).

Prognosis for non-alcoholic fatty liver disease

With progression non-alcoholic fatty liver disease There is a higher risk of developing cardiovascular diseases, atherosclerosis, metabolic syndrome, and type 2 diabetes.

Overall for non-alcoholic fatty liver disease characterized by a benign course. The development of liver cirrhosis is observed in only 5% of cases. The prognosis of the disease is influenced by such factors as the presence of concomitant pathology, primarily obesity, diabetes mellitus, dyslipidemia, arterial hypertension and adequate correction of metabolic disorders.

Treatment of liver steatosis

• Weight loss, lifestyle changes (diet and exercise).
• Treatment of metabolic syndrome.
• Use of hepatoprotectors.
• Restoration of intestinal microflora.
• Correction of lipid metabolism.

When the doctor and patient work together, treatment liver steatosis goes well. GUTA CLINIC has its own extensive diagnostic base for identifying non-alcoholic fatty liver disease at any stage. We use expert-level equipment from the world's leading manufacturers - leaders in the production of medical devices. Highly qualified doctors of GUTA CLINIC, candidates and doctors of medical sciences, using their rich clinical experience, will prescribe an individual regimen treatment of liver steatosis and help you stay healthy!

Although fat accumulation in the liver occurs in fairly thin people, obesity and the presence of type II diabetes mellitus are the main factors for this disease. The direct relationship between insulin resistance and steatosis (fat accumulation) suggests metabolic disorders in the body that underlie this disease.

In addition to the accumulation of incoming lipids, due to disruption of metabolic processes, the liver itself begins their increased synthesis. Unlike alcoholic fatty liver disease, the non-alcoholic form can occur in people who do not drink alcohol, have not undergone surgery, or take medications.

In addition to metabolic factors, the causes of fat accumulation can be:

• Surgical operations associated with weight loss (gastroplasty, or gastric anastomosis)
• Medicines:

1. Amiodarone
2. Methotrexate
3. Tamoxifen
4. Nucleoside analogues

• Parenteral nutrition, or malnutrition (for celiac disease)
• Wilson-Konovalov disease (copper accumulation)
• Damage from toxins (phosphorus, petrochemicals)

Symptoms

In most people, steatohepatosis (fatty liver inflammation) is asymptomatic until the terminal stages. Therefore, people prone to obesity and suffering from type II diabetes mellitus (main risk groups) need to regularly undergo ultrasound examinations of this organ.

Among the specific symptoms that arise are:

• Increased fatigue
• Pain in the right hypochondrium

These symptoms of non-alcoholic fatty liver are often confused with gallstones. The persistent appearance of the liver during removal of the gallbladder (cholecystectomy), or the pathological condition during the operation itself is an indication for consultation with a hepatologist.

As the disease progresses, spider veins may appear on the arms and body, and palmar erythema (redness of the palmar surface of the hand) is also characteristic.

Stage 1 (fatty hepatosis)

A healthy liver contains lipids in amounts not exceeding 5% of its mass. In the liver of an obese patient, both the amount of triglycerides (unsaturated fatty acids) and free fatty acids (saturated) increases. At the same time, the transport of fats from the liver decreases and their accumulation begins. A whole cascade of processes is launched, as a result of which lipids are oxidized with the formation of free radicals that damage hepatocytes.

As a rule, the first stage proceeds unnoticed. It can last several months, or even years. Damage occurs gradually and does not affect the main functions of the organ.

Stage 2 (metabolic steatohepatitis)

Due to cell damage (due to fatty degeneration of the liver), inflammation develops - steatohepatitis. Also during this period, insulin resistance increases and the breakdown of fats is suppressed, which increases their accumulation. Metabolic disorders begin, which lead to the death of hepatocytes (the level of aminotransferases in the blood increases - the first diagnostic sign).

Possessing high regenerative abilities, the liver itself replaces damaged cells. However, necrosis and progressive inflammation exceed the compensatory capabilities of the organ, leading to hepatomegaly.

The first symptoms appear in the form of fatigue, and with a sufficient increase in the size of the liver, pain appears in the right hypochondrium.

The parenchyma of the organ itself does not contain nerve endings. Pain occurs when the fibrous capsule of the liver begins to stretch due to inflammation and hepatomegaly.

Stage 3 (cirrhosis)

Cirrhosis is an irreversible process in which a diffuse proliferation of connective tissue occurs in the liver and replaces the normal parenchyma of the organ. In this case, areas of regeneration appear that are no longer able to restore the liver, since the new hepatocytes are functionally defective. Portal hypertension gradually develops (increased pressure in the liver vessels) with further progression of liver failure until complete organ failure. Complications appear from other organs and systems:

• Ascites is the accumulation of fluid in the abdominal cavity.
• Enlarged spleen with the development of anemia, leukemia and thrombocytopenia.
• Haemorrhoids.
• Endocrine disorders (infertility, testicular atrophy, gincomastia).
• Skin disorders (palmar erythema, jaundice).
• Hepatic encephalopathy (damage to brain toxins).

In cases of severe cirrhosis, the only treatment option is a donor liver transplant.

Treatment

The most difficult aspects of the treatment of non-alcoholic fatty liver disease are the individual selection of therapy for the patient and the risk-benefit ratio in each method. The main treatment measures are diet and increased physical activity. This is part of the usual recommendations for creating a healthy lifestyle, which, despite the different attitudes of the patients themselves, improves the patient’s quality of life and increases the effectiveness of other methods.

It is also important to treat the underlying disease that led to liver damage.

Diet

The composition of fats included in the diet may be of particular importance for patients with diabetes, since fatty acids (saturated fats) affect the sensitivity of cells to insulin.

Also, increasing the level of fatty acids accelerates fat metabolism and leads to a decrease in fatty inflammation. Therefore, the optimal ratio of fats is considered to be 7:3 animal and vegetable, respectively. In this case, the daily amount of fat should not exceed 80-90 grams.

Normalization of physical activity

When losing body weight through exercise and diet, it is important to follow stages, since weight loss of more than 1.6 kg/week can lead to progression of the disease.

The type of physical activity is determined taking into account concomitant diseases, the level of physical development and the severity of the patient’s condition. However, regardless of the factors, the number of classes per week should not be less than 3-4 times, 30-40 minutes each.

The most effective are considered to be loads that do not exceed the lactate threshold, that is, they do not contribute to the production of lactic acid in the muscles, and therefore are not accompanied by unpleasant sensations.

Drug treatment

The main goal of drugs is to improve the condition of the liver parenchyma (reduce inflammation and steatosis, stop the processes of fibrosis of the liver parenchyma).

Apply:

• Thiazolidones (troglisatone, pioglizatone)
• metformin
• cytoprotectors (ursodeoxycholic acid)
• vitamin E (often combined with vitamin C)
• pentoxifylline
• antihyperlipidemic drugs (fibrates)

These drugs are prescribed in long cycles of 4 to 12 months. Thiazolidones increase cell sensitivity to insulin, increasing glucose utilization and reducing its synthesis in adipose tissue, muscles and liver.

Metformin is an antihyperglycemic drug and is often used in combination with other medications. Although metformin has a low risk of hypoglycemia, it is used cautiously in combination with exercise and a low-carbohydrate diet.

Ursodeoxycholic acid is prescribed not only for steatohepatosis, but also as a preventive measure for the development of stones in the gallbladder. In addition to hepatoprotective functions, it is a choleretic agent, which also improves liver function.

Being a fat-soluble vitamin, vitamin E accumulates well in the liver, protecting it from external negative influences and normalizing the metabolism of hepatocytes. The combination with vitamin C helps eliminate the toxic effects of other medications, as both vitamins are antioxidants.

Pentoxifyline leads to the development of oxidative stress, during which lipids are broken down, reducing toxic and inflammatory processes in the liver.

Fibrates act on the receptors of the liver, heart, muscles and kidneys, increasing the breakdown of fats in them and preventing subsequent accumulation.

If a diet is ineffective for weight loss, orlistat may be prescribed. It is a synthetic analogue of lipostatin, which is produced in the human body and blocks lipase, and also reduces the absorption of fats in the intestines. Prescribed under the strict supervision of a physician.

Traditional methods

Decoctions of rowan, blackberry and sea buckthorn are widely used at home. These berries, like nuts, contain natural vitamin E, which is a hepatoprotector. The benefits of vitamin E are enhanced by foods containing vitamins C (citrus fruits) and A (carrots).

Vitamin E is a fat-soluble vitamin, so it is better absorbed with natural fats: butter, seafood, meat, olive oil, legumes and nuts.

If you already take these vitamins in dosage forms, you should not increase their amount in your diet. Do not forget that hypervitaminosis, unlike hypovitaminosis, is less treatable and has irreversible consequences for the body.

Increasing your diet with oatmeal and honey also has a positive effect on the liver.

Medicinal herbs and berries that work well include:

• mint or lemon balm teas;
• rosehip infusions;
• infusions with tansy;
• coriander extract;
• hawthorn teas;
• milk thistle extract.

Many of the above herbs lower blood pressure and are contraindicated for hypotensive patients.

You should also not use traditional medicine in large quantities. Stick to the recipe, as the difference between medicine and poison is often only in the dosage.

For quotation: Makhov V.M., Volodina T.V., Panferov A.S. Alcoholic and non-alcoholic fatty liver disease – we also take into account cavity digestion // Breast Cancer. 2014. No. 20. S. 1442

The organ-nosological approach to diagnosis and treatment in gastroenterology leads to the fact that diseases of the liver, biliary tract (BDT), and pancreas (PG) are considered separately. Problems caused by the anatomical and physiological relationships of the organs of the digestive system may fade into the background. The loss of any link in the system causes a cascade of subsequent changes. Common etiological factors also lead to comorbid pathology: alcohol, lipid and carbohydrate metabolism disorders, protein deficiency in the diet, viral and bacterial infection.

The most attention is drawn to the “friendly” pathology of the liver and pancreas - the main participants in the processes of digestion and metabolism. Such simultaneous involvement is defined by the concept of “hepatopancreatic syndrome”.
In therapy, the need to take into account the consequences caused by simultaneous dysfunction of the liver and pancreas arises in pathologies that have significant common pathogenetic bases - in alcoholic fatty liver disease (AFLD) and non-alcoholic fatty liver disease (NAFLD). The most important consequence of a systemic combination of organ dysfunctions is a violation of cavity digestion
The liver, pancreas, and gastrointestinal tract are most susceptible to the pathological effects of alcohol. Manifestations of damage to the digestive organs during chronic alcohol intoxication (CAI) have a number of features: the severity of the damage directly correlates with the duration of alcoholism, the pathology of the gastrointestinal tract has a multi-organ systemic nature; the development, sequence and degree of involvement in the process are largely determined by the anatomical and functional relationship of the organs.
A number of factors lead to simultaneous damage to the digestive organs in CAI, such as:
. the same type of effect of alcohol on cells and organs;
. single channel (digestive tube);
. interdependent participation in the digestive process;
. systemic nature of metabolism;
. commonality of neurohumoral regulation.
With daily alcohol consumption in quantities exceeding 40-60 g (for men) and 20 g (for women), morphological changes occur in the liver, united by the concept of “alcoholic liver disease” (ALD).
Clinically and experimentally, a direct relationship between the severity of liver damage and the duration of CAI and the amount of ethanol has been shown. Morphological changes in the liver with CAI go through the following stages:
. fatty degeneration;
. hepatitis (acute, chronic);
. fibrosis;
. cirrhosis.
In fatty liver disease (FLLD), the amount of fat, mainly triglycerides (TG), reaches more than 5% of the dry matter of the organ. LDP accounts for up to 85% of all liver pathology caused by alcohol. It is emphasized that HDP is not accompanied by inflammatory infiltration of the portal tracts.
Alcohol is oxidized to acetaldehyde with the participation of the enzyme alcohol dehydrogenase (ADH): 10-15% in the gastric mucosa, 80-85% in the liver, 5% is excreted unchanged in the urine. Acetaldehyde is highly toxic. The pathogenic effect depends on the amount of acetaldehyde formed in the cytosol, which is primarily due to the volume of incoming alcohol and the rate of its oxidation. The rate of ethanol oxidation is directly related to the activity of the ADH isoenzymes present in an individual. The amount of acetaldehyde found in the liver depends both on the rate of its formation and on the rate of further metabolism. Acetaldehyde, with the participation of aldehyde dehydrogenase, is transformed into acetyl-CoA, then either into acetate, followed by metabolism to carbon dioxide and water, or, entering the citric acid cycle, into other compounds, including fatty acids.
In case of fatty degeneration, cessation of alcohol intake in the absence of other hepatotoxic factors leads to complete morphological normalization of the hepatocyte.
The pathogenesis of TG accumulation in the liver in fatty degeneration of any etiology includes the following main links:
. increased intake of free fatty acids (FFA);
. increased lipid synthesis in hepatocyte mitochondria;
. decreased activity of lipid β-oxidation in hepatocyte mitochondria;
. slowing down the elimination of TG from the liver.
Alcohol in the liver tissue as an organic solvent can damage the membranes of cells and mitochondria, but the leading factor in the development of alcoholic LDP (ADP) is considered to be a high and long-term concentration of acetaldehyde in the liver tissue and the associated high content of nicotinamide adenine dinucleotide. At the same time, peripheral lipolysis is intensified, and the uptake of fatty acids by the liver increases. An excessive increase in the number and size of fatty inclusions in a hepatocyte leads to a fatal disruption of the metabolism of the liver cell and its death, i.e. to steatonecrosis.
Necrosis is caused by the initiation of lipid peroxidation (LPO) with the participation of acetaldehyde. Activation of LPO leads to an increase in oxygen demand in the hepatic lobule and the development of hypoxia, especially in the centrilobular zone. Important in understanding the pathogenesis is the effect of acetaldehyde binding to phospholipids (PL), which leads to the destruction of the cell membrane and mitochondrial membranes.
It can be assumed that, against the background of depletion of antioxidant protection in CAI, alcohol excess, especially in combination with fatty foods, can serve as an impetus for the development of oxidative stress.
J. Ludwig et al. in 1980, when examining the liver of persons who did not abuse alcohol, they found a histological picture identical to that of alcoholic hepatitis. The dynamics of this etiological variant of liver pathology, called NAFLD, are similar to alcoholic: NAF (non-alcoholic steatosis) - non-alcoholic steatohepatitis (NASH) - liver cirrhosis.
Criteria for the diagnosis of NAFLD:
. puncture biopsy data: gastrointestinal tract or inflammatory changes similar to changes in alcoholic hepatitis;
. no alcohol consumption in hepatotoxic doses;
. absence of other liver pathology.
In Russia in 2007, a screening program was carried out to identify the prevalence of NAFLD and determine risk factors for the development of this disease. In a study of 30,787 patients in the clinic, NAFLD was noted in 26.1% of patients. In this group, HDP was detected in 79.9%, NASH in 17.1%, liver cirrhosis in 3%.
Traditionally, there are 2 stages (2 “pushes”) of the pathogenesis of NAFLD. The first is caused by a violation of carbohydrate and lipid metabolism. At the same time, the high role of insulin resistance in the pathogenesis of NAFLD and NASH is noted. It has been noted that NAFLD is often accompanied by metabolic syndrome, in which insulin resistance is the leading link.
In accordance with the stages of pathogenesis, primary and secondary NAFLD are distinguished. In primary NAFLD, when the etiological factors are obesity, type 2 diabetes mellitus (DM), and dyshyperlipidemia, high levels of TG, lipoproteins and FFA are detected in the blood and liver. The accumulation of FFAs in the liver contributes to high blood insulin levels; hyperinsulinism, which accompanies obesity, type 2 diabetes and metabolic syndrome, is a pathogenetic factor, since insulin stimulates the synthesis of FFA, TG, and also reduces the rate of β-oxidation of FFA and the evacuation of lipids from the liver. It is assumed that the “first impulse” in the primary variant of NASH is the accumulation of FFA in the hepatocyte. FFAs are a highly reactive LPO substrate. This process with the formation of active radicals leads to damage to mitochondria and cell membranes.
There has been an understanding that only excessive accumulation of FFAs in the liver is necessary, but not sufficient, for the occurrence of oxidative stress. The idea of ​​a “second shock” leading to NASH and a secondary variant of NAFLD was formulated. The influence of drugs, deficiency of antioxidants in food, and hormonal imbalance are considered as inducers, additional factors of the “second push”.
The list of diseases and situations in which “secondary” NAFLD and NASH occur is very wide and includes: malabsorption syndrome, especially during surgery for obesity; intensive weight loss; long-term, unbalanced parenteral nutrition; storage diseases. Medicines that are often associated with the development of NASH have also been identified: amiodarone, glucocorticosteroids, tetracycline, non-steroidal anti-inflammatory drugs, methotrexate, synthetic estrogens, tamoxifen.
Thus, the common links in the pathogenesis of ALD and NAFLD can be traced: first of all, activation of lipid peroxidation, oxidative stress, damage to PL of mitochondrial membranes, disruption of systemic and cellular components of lipid metabolism. It is also possible to assume a “crossover” of predisposing factors: alcoholism, obesity, insulin resistance, hyperlipidemia, intestinal digestive disorders.
ZhDP is characterized by diffuse pathological intracellular fat deposition - often large droplets. Depending on the intensity of steatosis, hepatocytes function normally or steatonecrosis develops. ZhDP, as a rule, is asymptomatic; patients come under the supervision of a doctor by chance, when hepatomegaly is detected. Functional liver tests are slightly changed: in 1/3 of patients, slight unconjugated hyperbilirubinemia, high levels of cholesterol and TG in the blood are detected. An increase in the activity of ALT and AST, g-glutamyl transpeptidase is observed in less than half of the observations and follows alcohol excess.
Sometimes patients complain of anorexia, discomfort and dull pain in the right hypochondrium or epigastrium, nausea. By palpation it can be determined that the liver is enlarged, smooth, with a rounded edge. Ultrasound diagnoses diffuse moderate hyperechogenicity of the liver parenchyma structure. The diagnosis must be confirmed histologically.
The pancreas is more sensitive to alcohol, and therefore the so-called amount of alcohol for the pancreas that is relatively safe for the liver should be reduced by 2 times for men, and by 3 times for women. The concentration of alcohol in the cells of the pancreas reaches 60% of its concentration in the blood. As a result of direct exposure to ethanol, fatty infiltration of the pancreas appears, which occurs due to an increase in the synthesis of fatty acids and a decrease in their oxidation. There is also an increase in collagen production due to an increase in the activity of glycyl-propyl-dipeptide amino-peptidase. In this case, the direct effect of alcohol on the large duodenal nipple is accompanied by a spasm of the sphincter of Oddi.
Drinking alcohol in hepatotoxic doses always leads to the development of alcoholic chronic pancreatitis (ACP). Clinical instrumental research allows us to identify all forms characteristic of chronic pancreatitis (CP) in CAI. The progression of ACP leads to the formation of calcifications in the gland, the development of steatorrhea and diabetes. Quitting alcohol does not lead to normalization of the structure of the pancreas.
The development of AFL and ACP is combined with a violation of the state of the gallbladder. Thus, ultrasound of 286 patients with CAI revealed deformation of the gallbladder in 31% of those examined, thickening and compaction of the bladder wall - in 58 and 51%, respectively, and ultrasound dynamic cholecystography diagnosed hypomotor dyskinesia in 48%. Gastroduodenoscopy revealed papillitis in 52% and sphincter of Oddi insufficiency in 22% of patients. Thus, there is an important circumstance: in ACP, pathogenesis factors that are also inherent in bi-dependent CP are often found. Thus, during endoscopic retrograde cholangiopancreatography for ACP, choledochopancreatic reflux was detected in 8%, and narrowing of the terminal portion of the common bile duct - in 20% of cases.
In the clinical picture of AFLD, a significant role is played by the systemic, multi-organ consequences of CAI: CP with exocrine insufficiency, chronic atrophic gastritis, which lead to maldigestion. Bacterial overgrowth in the small intestine aggravates intestinal dyspepsia.
Eating behavior disorders and disorders of carbohydrate and lipid metabolism can also be considered as common factors in the development of AFLLD and NAFLD. One-third of patients with ADLD have an increased body mass index. This is explained by additional alcohol calories (1.0 g of ethanol - 7 kcal), stimulation of acid production by alcohol, leading to increased appetite, as well as uncontrolled consumption of food with excess animal fats and spicy snacks. With “hungry” drunkenness, there is a deficiency of proteins in the diet, as well as a lack of unsaturated fatty acids, antioxidants, and vitamins. An increase in the content of TG and cholesterol in the blood was also noted in CAI. A study of blood levels of insulin and C-peptide in alcoholism demonstrated true hyperinsulinemia.
One of the criteria for the diagnosis of NASH is the absence of alcohol consumption in hepatotoxic doses, i.e., identification of NASH is based on determining the amount of alcohol consumed. It should be borne in mind that a conversation with a patient rarely gives an accurate idea of ​​the amount of alcohol consumed.
With alcoholic origin, the following can be observed: dilation of nasal vessels, scleral injection, erythema of the palms, as well as enlargement of the parotid glands, gynecomastia, and Dupuytren's contracture. Physical examination data are uninformative.
In alcohol-associated pathology, complaints of pain are less pronounced; it is believed that this is the effect of the analgesic, antidepressant, and euphoric effect of ethanol.
With AFLD, there may be symptoms included in the “weekend syndrome”, when on Monday (after drinking alcohol on Friday and Saturday) asthenic syndrome and syndromes of gastric and intestinal dyspepsia occur. With NAFLD, patients present complaints, most often caused by dyskinesia of the gallbladder, characteristic of functional gastric dyspepsia in the form of either epigastric pain syndrome or postprandial distress syndrome.
With alcoholic steatohepatitis (ASH), symptoms of intestinal dyspepsia are more often observed, with NASH - signs of involvement of the gallbladder in the pathological process.
Objective markers of CAI are the results of laboratory tests:
. increased activity of γ-glutamyl transpeptidase (GGT) in the blood;
. increased levels of class A immunoglobulins in the blood;
. increase in average red blood cell volume;
. an increase in AST activity in the blood, exceeding ALT activity;
. increased levels of transferrin (carbon-deficient) in the blood.
Laboratory indicators of cytolysis in ASH depend on the time elapsed since alcohol consumption, but the level of GGT in ASH is noticeably higher than in NASH. This occurs due to the manifestation of canalicular cholestasis in the centrilobular zone.
The course and prognosis of both NASH and ASH are also determined by the presence of common progression factors, such as high obesity, hypertriglyceridemia, insulin resistance, high activity of liver enzymes, old age, and malnutrition. The combination of etiological factors of ALD and NAFLD is defined as comorbidity. Prohibition of alcohol intake is considered mandatory in the treatment of both AFLD and NAFLD.
The comorbidity of AFL and ACP, as well as coexisting dysfunction of the gallbladder, are serious causes of disturbances in cavity intestinal digestion. Steatorrhea is included in the diagnostic triad of ACP: calcifications, steatorrhea, diabetes. Alcoholization is accompanied by a higher rate of decline in the excretory function of the pancreas. In NAFLD, circumstances have also been identified that contribute to the development of intestinal maldigestion. It has been shown that the accumulation of lipids in the hepatocyte in NAFLD leads to a decrease in the production of primary bile acids and their entry into the duodenum (duodenum) with bile. The course of diabetes is accompanied by various manifestations of gastroenterological disorders and complications. A number of researchers demonstrate a decrease in GB contractility in patients with diabetes.
A test to determine elastase-1 revealed a decrease in enzyme excretion in more than 1/3 of patients with diabetes, and the risk of pancreatic failure is higher with a combination of diabetes and obesity.
The positive effect of pancreatic enzyme replacement therapy on the structural and functional state of the liver in NAFLD has been demonstrated. The presence of similar links in pathogenesis allows us to discuss common positions in approaches to the treatment of ALD and NAFLD.
Since obesity and insulin resistance are the main factors in the development of NAFLD and NASH, the main goals of non-drug therapy are to reduce calories in the diet due mainly to fats and carbohydrates, and increase physical activity. Weight loss is individualized. General principles: slow weight loss (1.5-2 kg per month); sharp restriction of intake of simple carbohydrates and saturated fats. The diet should include a sufficient amount of dietary plant fiber (30-40 g/day); it is advisable to use wheat bran and flax seed.
Stopping drinking alcohol is an important factor in treatment. It is believed that 1/3 of patients stop drinking alcohol, 1/3 only reduces the dose, and 1/3 continues to drink it in the usual amount. People who stop drinking, as a rule, have low tolerance, no hangover syndrome or its weak manifestation, suspicious people (coding!) and people with high social status.
Continued alcohol consumption is not a reason to refuse treatment. It was demonstrated that the use of essential PL (EPL) along with a decrease in the dose of alcohol reduced the rate of fibrosis formation in patients compared to those receiving placebo.
The most important pathogenetically substantiated, well-proven remedy aimed at eliminating the damaging effects of the main links in the pathogenesis of HDP is EPL.
EPL is phosphatidylcholine, which contains polyunsaturated fatty acids, mainly linoleic (about 70%), as well as linolenic and oleic. Phosphatidylcholine, which contains a large amount of polyunsaturated fatty acids, is also referred to as polyenylphosphatidylcholine (PPC). A healthy person receives polyunsaturated fatty acids from food, mainly from vegetable oils. For industrial purposes, PPC is extracted from soybeans to create medicines. PRS contains 1,2-dilinoleoylphosphatidylcholine, which has the highest bioavailability and is the active ingredient of EPL.
A medicinal product containing 300 mg of EPL in 1 capsule is Essentiale® forte N.
Essentiale® forte N occupies a leading position in the group of hepatoprotectors. The drug has been widely and successfully used in many countries around the world for more than 50 years. The effectiveness and safety of Essentiale® forte N have been demonstrated in a large number of clinical studies, including, importantly, double-blind studies. The drug Essentiale® forte N is the most studied among drugs containing EPL.
The positive effect on the metabolism of cell membranes and mitochondria, the antioxidant effect, and the normalizing effect on lipid metabolism were the key to the successful use of Essentiale® forte N in AFLLD and NAFLD, taking into account the “crossover” of pathogenesis. Moreover, it has been shown that the content of phosphatidylcholine in patients with NAFLD is significantly reduced compared to that in healthy individuals.
Cavity digestion in both AFLD and NAFLD is affected by factors leading to impaired breakdown of nutrients. Detection of cavity digestion disorders with the development of maldigestion is the predominant indication for prescribing multienzyme replacement therapy.
In AFLLD, the prevailing causes of intestinal dyspepsia are a decrease in the external secretion of the pancreas and defects in the functioning of the gallbladder; in NAFLD, changes in the composition of bile, dyskinesia of the gallbladder and disturbances in enteral enzyme production predominate.
In such clinical situations, it is advisable to prescribe combined replacement agents containing pancreatin, bile and hemicellulose. Such means include the well-proven Festal. One tablet, coated with an acid-resistant coating, contains 192.0 mg of pancreatin. In International Pharmaceutical Federation units, this amount is equivalent to 6000 units of lipase, 4500 units of amylase, 300 units of protease. The drug also includes hemicellulase - 50.0 mg and bile components - 25.0 mg.
Festal's pancreatin, having entered the duodenum, is included in intestinal digestion, compensating for the lack of enzymes or supplementing pancreatic enzymes. The presence of bile acids and hemicellulase in the drug significantly expands the range of effectiveness of the drug. Festal's bile acids independently emulsify fats in case of reduced production of primary bile acids by the liver, as well as in case of inadequate or uncoordinated flow of bile into the duodenum. Thus, bile replacement therapy takes place.
It should be noted that Festal bile acids stimulate the secretory activity of the pancreas and accelerate intestinal motility. They are true choleretics and help increase the flow of bile into the intestines. This is accompanied by an intensification of the bactericidal effect of bile and a decrease in contamination.
An important point that requires special discussion when taking the drug is stimulation of the exocrine function of the pancreas. It is clear that for painful chronic and acute pancreatitis, such an effect is unacceptable; the drug is not recommended for exacerbation of CP. The list of contraindications due to the presence of bile includes hyperbilirubinemia, obstructive jaundice and empyema of the gallbladder.
Hemicellulase in the drug helps reduce intestinal dyspepsia. The enzyme breaks down plant fiber polysaccharides, which reduces gas formation and is clinically manifested by a decrease in flatulence.
Analysis of Festal's capabilities allows its use in AFL and NAFLD along with Essentiale® forte N. Therapy with Essentiale® forte N is pathogenetically substantiated and acceptable for any etiology of fatty degeneration. The need to introduce a course of Festal is determined by the state of the external secretion of the pancreas, the bile-forming function of the liver, and the tone of the pancreas.
The duration of the combined course of Essentiale® forte N and Festal is determined as follows: Essentiale® forte N is taken 2 capsules 3 times a day for at least 3 months, courses are repeated 2-3 times a year. The duration of Festal therapy is determined by the clinical picture of intestinal dyspepsia, the degree of steatorrhea, and the status of the gallbladder on ultrasound and can range from 3-4 weeks. up to several months.
Combination therapy with Essentiale® forte N and Festal is advisable for a combination of gastrointestinal tract, primary or secondary exocrine pancreatic insufficiency, and gallbladder dysfunction.
The pathogenetically substantiated combined use of Essentiale® forte N and Festal makes it possible to optimize the treatment of gastrointestinal tract of any etiology in combination with pancreatic and biliary insufficiency.

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Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic pathologies nowadays. It can also be one of the signs of metabolic syndrome, type II diabetes mellitus and obesity.

The term “non-alcoholic steatohepatitis” was first proposed in 1980. When studying liver preparations from patients who did not drink alcoholic beverages in hepatotoxic doses, changes characteristic of alcoholic liver damage were discovered.

The term NAFLD contains three successive stages:

• non-alcoholic steatosis (fatty hepatosis);
• non-alcoholic (metabolic) steatohepatitis (NASH);
• cirrhosis as an outcome of NASH progression.

It is extremely rare for non-alcoholic steatohepatitis to transform into hepatocellular cancer.

According to the literature, unfavorable outcomes of this disease, in the absence or insufficient treatment, are not so rare. Almost half of the cases develop cirrhosis, and about 5% develop hepatocellular carcinoma.
Very often, non-alcoholic fatty liver disease is detected by chance - during a biochemical blood test, or changes are detected on an ultrasound examination of the abdominal cavity.

Relevance of the problem

The frequency of non-alcoholic fatty liver disease in the population is not reliably known due to its hidden course and associated difficulties in early diagnosis. However, according to recent studies, the prevalence of this disease in the form of steatosis can be over 25% (in some regions more than 50%), and non-alcoholic steatohepatitis - up to 5%.

In diseases that are accompanied by insulin resistance (metabolic syndrome, type II diabetes mellitus, obesity, dyslipidemia), specific transformations in the liver are detected in approximately 75% of cases, and with concomitant obesity - up to 95%.

Nowadays, there is an increase in the incidence of morbid obesity among the world population, in particular in developed countries. This is facilitated by physical inactivity, improper and unbalanced nutrition. Due to this, the number of cases of NAFLD is also increasing.

Patients diagnosed with metabolic syndrome have the greatest risk of the occurrence and progression of this pathology.

According to WHO, cardiovascular diseases are in first place among the causes of death in the world. Patients suffering from NAFLD have an increased risk of developing pathologies of the heart and blood vessels, which is confirmed by numerous studies in this area.

NAFLD most often affects women aged 40–60 years, as well as patients with manifestations of insulin resistance, in particular metabolic syndrome. But the incidence is observed in different age categories. Children are no exception: this pathology is diagnosed in about 3% of all children, and in obese children the disease rate reaches 55%.

Relationship between non-alcoholic hepatosis and metabolism

The pathogenesis of NAFLD is still being studied, but the following conclusions have already been drawn: one of the main roles in this is played by the phenomenon of insulin resistance. What kind of disease is this and why is it dangerous?

Insulin resistance is a condition that is characterized by a decrease (up to complete absence) in the sensitivity of the body's peripheral tissues to the biological effects of insulin.

It does not matter where it comes from: in the process of synthesis by the pancreas (endogenous) or from the outside (exogenous). As a result, an increased concentration of insulin in the blood is created. It is known that insulin has a direct effect on carbohydrate and lipid metabolism, and also acts on the vascular endothelium.

As a result of a prolonged increase in the amount of insulin in the body, various metabolic disorders occur. As a result, type II diabetes mellitus, cardiovascular diseases, etc. may develop.

The causes of insulin resistance are not fully understood. There is a frequent development of decreased sensitivity of cellular receptors to insulin in people with excess body weight and a tendency to develop arterial hypertension. The reason is the tendency of adipose tissue to increase metabolic activity, for example, if body weight is 35-40% more than normal, then insulin sensitivity will decrease by 40%.

Assessment of immunoresistance using the HOmeostasis Model Assessment (HOMA) index
In practical medicine, the HOMA index is used: fasting blood glucose (mmol/l) × insulin (µU/ml) / 22.5. When the HOMA index is above 1.64, a person is diagnosed with insulin resistance.

Tissue resistance to insulin underlies the metabolic syndrome; in addition, an increase in the amount of visceral fat, arterial hypertension, and disruptions in lipid, carbohydrate and purine metabolism play a role.

There are clear criteria for diagnosing metabolic syndrome according to the International Diabetes Federation (IDF). Abdominal obesity must be present in combination with any two of the following conditions:

• increase in triglycerides;
• lowering the fraction of “good” cholesterol - high-density lipoproteins (HDL);
• development of arterial hypertension;
• there is impaired glucose tolerance or type II diabetes mellitus.

Treatment of metabolic syndrome is symptomatic; in addition, it is necessary to change your lifestyle and diet. The main points are:

• getting rid of excess weight, possible drug treatment of obesity;
• physical activity and the fight against physical inactivity are required;
• arterial hypertension therapy;
• treatment of impaired glucose tolerance and type II diabetes mellitus;
• correction of impaired lipid metabolism (dyslipoproteinemia).

Insulin resistance can exist without the presence of the complex that characterizes metabolic syndrome. For example, 10% of people with this pathology do not have any metabolic disorders.

One of the manifestations of metabolic disorders, due to a decrease in the sensitivity of insulin receptors, is a disorder of lipid metabolism (dyslipidemia).
Triglycerides accumulate in the liver tissue and cause the formation of steatosis. The degree of fatty infiltration depends on the percentage of hepatocytes that have accumulated fat deposits:

1. soft - up to 30%;
2. moderate - from 30 to 60%;
3. pronounced - more than 60%.

By eliminating the causes that caused these disorders, fat deposition in hepatocytes is significantly reduced. Steatosis is a reversible process.

As the disease progresses, free fatty acids are released from lipid tissue. These compounds, in combination with some other factors, contribute to the development of oxidative stress, which leads to inflammation and subsequent destruction of liver cells. There is a transition from steatosis to steatohepatitis.

Signs of NAFLD can also occur in people without clinical signs of metabolic syndrome. In this case, the leading role belongs to the phenomenon of dysbiosis (violation of the qualitative composition of the intestinal microflora). This disrupts the formation of compounds that are responsible for the process of synthesis of “bad” very low-density lipoproteins (VLDL).
Intestinal endotoxicosis, which occurs during dysbiosis, can be another cause of oxidative stress.

Clinical manifestations and diagnosis

The course of the disease is in the vast majority of cases asymptomatic, especially in the stage of steatosis. The impetus for further diagnostic search is accidentally detected elevated levels of liver transaminases or ultrasound signs of fatty liver degeneration. Moreover, these examinations are often performed for preventive purposes or for other diseases.

Sometimes the patient may present nonspecific complaints: weakness, fatigue, mild discomfort in the right hypochondrium. More specific complaints, such as nausea, vomiting, skin itching, severe pain, as well as icteric syndrome and manifestations of portal hypertension, occur already in advanced forms.

The patient's medical history should be carefully collected. It is worth asking the patient about alcohol abuse, uncontrolled use of hepatotoxic drugs, infection with hepatitis viruses and other reasons that can cause damage to hepatocytes.

During examination, an enlarged liver is palpable in most patients, and in some, the spleen is palpable.

Laboratory examination

A biochemical blood test is quite informative. Based on the results of the analysis, it is possible to determine the level of involvement of the liver in the pathological process. Main biochemical indicators:

• Observed (ALT, AST, alkaline phosphatase, GGT and some others). The detected increases in activity are most often moderate, no more than 3–5 times. The ALT/AST index usually does not exceed 2.
• Manifestations of dyslipidemia are increased levels of triglycerides and cholesterol with a predominance of “bad” lipoproteins (VLDL and LDL).
• Manifestations of carbohydrate metabolism disorders are impaired glucose tolerance or diagnosed type II diabetes mellitus.
• In the case of advanced forms of NAFLD, the amount of bilirubin in the blood may increase, signs of protein metabolism disorders may appear (for example, decreased albumin) and prothrombin time may increase, etc.

You should be aware that in some patients, liver transaminase activity levels are within normal limits or only slightly elevated, even at an advanced stage of the disease.

Instrumental examination

Ultrasound, computer or magnetic resonance imaging is used. These methods help to assess the degree of fatty liver disease, identify hepatomegaly, and help in diagnosing a possible complication - portal hypertension.

Helps differentiate steatosis from steatohepatitis, assess the degree and prevalence of fibrosis, and make a prognosis for the course of the disease. Unfortunately, this diagnostic method is not always available for various reasons.

Indications for mandatory puncture biopsy are:

1. age (from 46 years) manifestations of chronic liver cytolysis of unknown origin;
2. combination of chronic cytolysis of unknown etiology with signs of metabolic syndrome.

How is non-alcoholic hepatosis treated?

There are still no specific criteria and standards for drug therapy for NAFLD.
Correction of detected metabolic disorders is carried out. It is necessary to change your diet to a dietary one, increase activity or introduce sports activities, this will help prevent the development or progression of the process.

Any drug therapy in such patients should be carried out very carefully, especially with drugs that have a potentially hepatotoxic effect (corticosteroids, amiodarone, tamoxifen and others). Therefore, it is necessary to take into account the presence of NAFLD when treating concomitant diseases.

Basic therapy methods

For overweight and obese individuals, it is necessary to make dietary adjustments to reduce weight.
The calorie content of food is calculated using special methods, taking into account initial body weight, age, gender, and intensity of physical activity.

Weight loss should occur smoothly and gradually. A sharp decrease in body weight can provoke the development of acute non-alcoholic steatohepatitis due to the penetration of free fatty acids into the liver against the background of active breakdown of fat cells. A weekly weight loss of 600g for children and 1600g for adults is considered safe.

Key points:

• reduction in daily energy value (calorie) of the diet;
• limiting the mass fraction of fats in the diet (up to 30%);
• consumption of foods high in polyunsaturated fatty acids;
• cutting back on cholesterol-rich foods;
• exclusion of fried foods;
• patients with type II diabetes or impaired glucose tolerance should consume foods with a low glycemic index;
• eliminating alcohol and other bad habits;
• inclusion in the diet of foods rich in fiber, which have natural antioxidant properties.

Drugs

Combination regimens are used for the treatment of non-alcoholic hepatosis. Treatment may vary for each situation. Main list of drug categories:

• Drugs that increase the sensitivity of insulin receptors: biguanides (metformin) and thiazolidinediones (rosiglitazone, pioglitazone). Have a positive effect in patients with insulin resistance. However, scientific research is still underway for the widespread use of these drugs for the treatment of NAFLD.
• Lipid-lowering drugs. They are divided into two subgroups – fibrates and statins. Prescribed to people with lipid metabolism disorders that cannot be treated with other means.
• Antioxidants and hepatoprotectors. This group of agents includes tocopheryl acetate, N-acetylcysteine, betaine, silibinin, etc. Considering the important role of oxidative stress in the progression of NAFLD, the use of antioxidants gives a positive result. There is evidence that the combination of antioxidants and hepatoprotectors reduces the manifestations of dyspepsia and favors the regression of pathological changes in the liver.

Restoration of microflora

Particular attention is paid to the intestines and restoration of normal microbiocenosis. Considering the important role of bacterial hepatoendotoxins in intestinal dysbiosis in the pathogenetic chain of development of NAFLD, correction of intestinal microflora is recommended. For this purpose, probiotics are used in most cases. Antibacterial and antiseptic drugs for dysbiosis are used according to very strict indications.

Treatment of concomitant diseases and syndromes is recommended. Dispensary observation of such patients includes monitoring the levels of biochemical and metabolic parameters, anthropometric measurements once every 6 months, and ultrasound of the abdominal organs once a year.
Based on the examination data, therapy is adjusted if necessary.

In conclusion, it is worth saying that scientific research is still underway to develop optimal approaches to the treatment and prevention of NAFLD. All risk factors that can lead to liver damage should be taken into account and all possible measures should be taken to minimize these manifestations.